Mitigated NSAID-induced apoptotic and autophagic cell death with Smad7 overexpression
DC Field | Value | Language |
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dc.contributor.author | Lee, Ho-Jae | - |
dc.contributor.author | Park, Jong Min | - |
dc.contributor.author | Hahm, Ki Baik | - |
dc.date.available | 2020-02-27T20:41:02Z | - |
dc.date.created | 2020-02-07 | - |
dc.date.issued | 2017-01 | - |
dc.identifier.issn | 0912-0009 | - |
dc.identifier.uri | https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/6541 | - |
dc.description.abstract | Non-steroidal anti-inflammatory drugs damaged gastrointestinal mucosa in cyclooxygenase-dependent and-independent pathway, among which apopototic or autophagic cell death in gastrointestinal cells might be one of key cytotoxic mechanisms responsible for NSAID-induced damages. Therefore, alleviating this cell death after NSAIDs can be a rescuing strategy. In this study, we explored the role of Smad7 on NSAID-induced cytotoxicity in gastric epithelial cells. Using RGM1 cells, we have compared biological changes between mock-transfected and Smad7-overexpressed cells. As results, significantly decreased cytotoxicity accompanied with decreased levels of cleaved caspase-3 and poly (ADP-ribose) polymerase, Bax, and autophagic vesicles concurrent with decreased expressions of autophagy protein 5 and microtubule-associated protein light chain 3B-II were noted in Smad7overexpressed cells with indomethacin administration compared to mock-transfected cells. Contrast to mitigated apoptotic execution, anti-apoptotic Bcl-2 and Beclin-1 were significantly increased in Smad7-overexpressed cells compared to mock-transfected cells. Smad7 siRNA significantly reversed these protective actions of Smad7 against indomethacin, in which p38 mitogen-activated protein kinase was significantly intervened. Furthermore, indomethacin-induced Smad7 degradation through ubiquitinproteasome pathway was relevant to increased cytotoxicity, while chloroquine as autophagy inhibitor significantly attenuated indomethacin-induced cytotoxicity through Smad7 preservation via repressed ubiquitination. Conclusively, either genetic over expression or pharmacological induction of Smad7 significantly attenuated indomethacin-induced gastric cell damages. | - |
dc.language | 영어 | - |
dc.language.iso | en | - |
dc.publisher | JOURNAL CLINICAL BIOCHEMISTRY & NUTRITION | - |
dc.relation.isPartOf | JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION | - |
dc.subject | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject | CANCER CELLS | - |
dc.subject | CHLOROQUINE | - |
dc.subject | INHIBITION | - |
dc.subject | DISEASE | - |
dc.subject | UBIQUITINATION | - |
dc.subject | CHEMOTHERAPY | - |
dc.subject | STRATEGIES | - |
dc.subject | DRUGS | - |
dc.title | Mitigated NSAID-induced apoptotic and autophagic cell death with Smad7 overexpression | - |
dc.type | Article | - |
dc.type.rims | ART | - |
dc.description.journalClass | 1 | - |
dc.identifier.wosid | 000397545800009 | - |
dc.identifier.doi | 10.3164/jcbn.16-69 | - |
dc.identifier.bibliographicCitation | JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION, v.60, no.1, pp.55 - 62 | - |
dc.identifier.scopusid | 2-s2.0-85007608374 | - |
dc.citation.endPage | 62 | - |
dc.citation.startPage | 55 | - |
dc.citation.title | JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION | - |
dc.citation.volume | 60 | - |
dc.citation.number | 1 | - |
dc.contributor.affiliatedAuthor | Lee, Ho-Jae | - |
dc.type.docType | Article | - |
dc.subject.keywordAuthor | NSAID | - |
dc.subject.keywordAuthor | gastrointestinal damages | - |
dc.subject.keywordAuthor | Smad7 | - |
dc.subject.keywordAuthor | apoptosis | - |
dc.subject.keywordAuthor | autophagy | - |
dc.subject.keywordPlus | ENDOPLASMIC-RETICULUM STRESS | - |
dc.subject.keywordPlus | CANCER CELLS | - |
dc.subject.keywordPlus | CHLOROQUINE | - |
dc.subject.keywordPlus | INHIBITION | - |
dc.subject.keywordPlus | DISEASE | - |
dc.subject.keywordPlus | UBIQUITINATION | - |
dc.subject.keywordPlus | CHEMOTHERAPY | - |
dc.subject.keywordPlus | STRATEGIES | - |
dc.subject.keywordPlus | DRUGS | - |
dc.relation.journalResearchArea | Nutrition & Dietetics | - |
dc.relation.journalWebOfScienceCategory | Nutrition & Dietetics | - |
dc.description.journalRegisteredClass | scie | - |
dc.description.journalRegisteredClass | scopus | - |
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